Ascending pyelonephritis in young rats retards kidney growth

Ascending pyelonephritis in young rats retards kidney growth. Several radiological studies have suggested that pyelonephritis in infancy and childhood may result in kidney growth retardation without renal scarring. In the present study, we induced ascending pyelonephritis in 20-day-old rats with intravesical infusion of E. coli. Four days after infusion, E. coli was cultured from all renal cortex. The rats were either left untreated (PNu) or were treated with trimethoprim-sulfa (PNt). The rats were investigated one month after infection and compared with an age-matched control group (C). Seventy-nine percent of the PNu rats had recovered spontaneously from infection. Body weight was the same in all groups. In PNu rats, kidney weight (KW), kidney area (KA) and glomerular filtration rate (GFR) were significantly decreased. KW, KA and GFR were similar in PNt and C rats. The numbers of filtering nephrons were not reduced by the infection. The total cortical DNA content (index of cell number) was significantly lower in PNu (5.30 ± 0.32 mg) and PNt (6.62 ± 0.44 mg) than in C rats (8.48 ± 0.49 mg). The cortical DNA content was significantly lower in PNu than in PNt rats. The cortical protein/DNA ratio was significantly higher in PNu rats than in C rats. The protein/DNA ratio was similar in PNt and PNu rats. The increase in protein/DNA ratio was interpreted as a sign of cell hypertrophy. The inflammatory process as such did not increase the protein/DNA ratio. The kidneys were also examined for structural lesions. Signs of scarring, inflammation and cell necrosis were almost absent in all groups. In conclusion, untreated pyelonephritis in young rats results in the reduction of the renal mass and GFR. The reduction of renal mass can be attributed to inhibition of cell mitosis. Cell mitosis can be inhibited even in cases where the pyelonephritis is treated, but a compensatory increase in cell size might then blunt the gross signs of renal growth retardation.